Diagnosed with SMM, SPB, or MGUS?

Learn how you can stall the development of full-blown Multiple Myeloma with evidence-based nutritional and supplementation therapies.

Click the orange button to the right to learn more.

Slow/Stop SMM’s March Toward Full-Blown Multiple Myeloma

Share Button

“Hyperdiploid-myeloma is associated with male sex, kappa immunoglobulin subtype, symptomatic bone disease and better survival compared to nonhyperdiploid-MM

Hi David-I contacted you a couple months back in regards to my husband 47yrs old who was diagnosed with SMM in July of this year. We are in contact with a local oncologist and also with a MM specialist at the MAYO CLINIC in AZ.

The specialist says my husband has Hyperdiploid MM. Which he says one of the less aggressive kinds. There was recently a study done that has not been published yet that determines if one will develop the active MM in 2 or 10 years based on whether or not they contain the Myc gene.

Recently we got the clinical lab results back on that. There was what he called a disruption in gene myc which suggests higher risk of early progression. The specialist recommends regardless of how the results come out there is nothing to be done till it does progress into active MM. Just quarterly blood tests.

We have changed my husbands diet drastically and he has been supplementing with turmeric. I should also mention he has no signs as of yet of MM. PET Scan, bone suryvey and MRI have all come back clear. I guess why I’m contacting you is because we are having a hard time coming to terms not being able to do anything till it progresses into active MM. In your opinion is anything else we can do? Diet, supplements whatever. We have 2 small children and will do anything for him to survive this and watch our babies grow. Thank you! Anne

Hi Anne,

Several things. The Mayo Clinic, both in AZ and Minnasota is a top-notch MM centers. In your case, seeing a MM specialist gave you superior diagnostic information. The good news is that your MM specialist is indicating that your husband’s prognosis is better than average. The bad news is that conventional oncology takes a “watch and wait” approach to pre-myeloma diagnoses such as smoldering myeloma.
Yes, there are evidence-based yet non-toxic therapies shown to reduce the risk of pre-myeloma patients progressing to full-blown MM. Curcumin is a good example of an evidence-based, non-toxic therapy. It is important to point out however, that it is essential for your husband to take one of the formulations that are more “bioavailable.” I credit my curcumin supplementation with keeping me in complete remission since April of 1999.

To learn more about these evidence-based, non-toxic therapies, please watch the short video below:


Let me know if you have any questions.
Thank you,
David Emerson
  • MM Survivor
  • MM Cancer Coach
  • Director PeopleBeatingCancer

“Chromosomal hyperdiploidy is the defining genetic signature in 40-50% of myeloma (MM) patients. We characterize hyperdiploid-MM (H-MM) in terms of its clinical and prognostic features in a cohort of 220 H-MM patients entered into clinical trials.
Hyperdiploid-myeloma is associated with male sex, kappa immunoglobulin subtype, symptomatic bone disease and better survival compared to nonhyperdiploid-MM (median overall survival 48 vs 35 months, log-rank P = 0.023), despite similar response to treatment.
Among 108 H-MM cases with FISH studies for common genetic abnormalities, survival is negatively affected by the existence of immunoglobulin heavy chain (IgH) translocations, especially those involving unknown partners, while the presence of chromosome 13 deletion by FISH did not significantly affect survival (median overall survival 50 vs 47 months, log-rank P = 0.47). Hyperdiploid-myeloma is therefore a unique genetic subtype of MM associated with improved outcome with distinct clinical features. The existence of IgH translocations but not chromosome 13 deletion by FISH negatively impacts survival and may allow further risk stratification of this population of MM patients.


“Myc is a family of regulator genes and proto-oncogenes that code for transcription factors. The Myc family consists of three related human genes: c-myc (MYC), l-myc (MYCL), and n-myc (MYCN). c-myc (also sometimes referred to as MYC) was the first gene to be discovered in this family, due to homology with the viral gene v-myc.

In cancer, c-myc is often constitutively (persistently) expressed. This leads to the increased expression of many genes, some of which are involved in cell proliferation, contributing to the formation of cancer.[1] A common human translocation involving c-myc is critical to the development of most cases of Burkitt lymphoma.[2] Constitutive upregulation of Myc genes have also been observed in carcinoma of the cervix, colon, breast, lung and stomach.[1] Myc is thus viewed as a promising target for anti-cancer drugs.[3] Unfortunately, Myc possesses several features that render it undruggable such that any anti-cancer drugs for Myc dysregulation will require acting on the protein indirectly, i.e. targeting the mRNA for the protein rather than a small molecule that targets the protein itself.[4][5]

In the human genome, C-myc is located on chromosome 8 and is believed to regulate expression of 15% of all genes[6] through binding on enhancer box sequences (E-boxes).

Leave a Comment: